Ultrasonographic Characteristics of the Adrenal Glands in Dogs With Pituitary-Dependent Hyperadrenocorticism: Comparison With Normal Dogs

Ultrasonographic evaluation of the adrenal glands was performed in 10 dogs with pituitary-dependent hyperadrenocorticism (PDH) and in 10 age- and weight-matched healthy control dogs. Thickness, shape, and echogenicity were determined for each adrenal gland. Adrenal thickness in dogs with PDH (median, 10 mm-left; 8.5 mm-right) was significantly greater than thickness in control dogs (median, 6 mm-left; 6 mm-right). Other ultrasonographic characteristics associated with PDH included bilaterally symmetrical adrenomegaly and maintenance of normal adrenal shape. Adrenal echogenicity was homogeneous and less than that of the adjacent renal cortex in 8 of 10 dogs with PDH and in 10 of 10 control dogs. Heterogenous echogenicity was present in 2 of 10 dogs with PDH, and was associated with nodular cortical hyperplasia in one of those dogs. Results of this study confirm the difference in sonographic appearance between PDH-induced bilateral cortical hyperplasia and functional adrenocortical neoplasia, and show a difference in so-nographically determined adrenal size between healthy dogs and dogs with PDH. J Vet Intern Med 1996; 10:110–115. Copyright © 1996 by the American College of Veterinary Internal Medicine .     

Indicators of malignancy of canine adrenocortical tumors: histopathology and proliferation index

Tumors of the adrenal cortex account for 10-20% of the naturally occurring Cushing's syndrome diagnosed in dogs. Differentiating between adrenocortical adenoma and carcinomas is often difficult. The purposes of this study were to determine which histopathologic criteria can be used as markers for malignancy in canine adrenocortical tumors and the relevance of the proliferation marker, Ki-67, for differentiation between cortical adenomas and carcinomas. Twenty-six adrenocortical carcinomas, 23 adenomas, and 11 normal adrenal glands were examined. Morphologic criteria significantly associated with adrenocortical carcinomas included a size larger than 2 cm in diameter, peripheral fibrosis, capsular invasion, trabecular growth pattern, hemorrhage, necrosis, and single-cell necrosis, whereas hematopoiesis, fibrin thombi, and cytoplasmic vacuolation were significantly associated with adrenocortical adenomas. The mean (+/- SD) proliferation index, measured by immunohistochemistry for the Ki-67 antigen, was 9.3 +/- 6.3% in carcinomas, 0.76 +/- 0.83% in adenomas, and 0.58 +/- 0.57% in normal adrenal glands. The Ki-67 proliferation index was significantly higher in carcinomas compared with adenomas and normal adrenal glands. A threshold value of the proliferation index of 2.4% reliably separated carcinomas from adenomas. Based on these results, it appears that thorough evaluation of morphologic features combined with immunohistochemical assessment of the proliferation index is extremely useful for differentiating between adrenocortical adenomas and carcinomas in dogs.     

Serum Inhibin Concentration in Dogs with Adrenal Gland Disease and in Healthy Dogs

Background

Studies in humans identified the synthesis and secretion of inhibin from adrenocortical tumors, but not pheochromocytoma (PHEO). Inhibin has not been examined in dogs as a serum biomarker for adrenal gland tumors.

Objective

To determine serum inhibin concentration in dogs with adrenal gland disease and in healthy dogs.

Animals

Forty‐eight neutered dogs with adrenal disease including pituitary‐dependent hyperadrenocorticism (PDH, 17), adrenocortical tumor (18), and PHEO (13), and 41 healthy intact or neutered dogs.

Methods

Prospective observational study. Dogs were diagnosed with PDH, adrenocortical tumor (hyperadrenocorticism or noncortisol secreting), or PHEO based on clinical signs, endocrine function tests, abdominal ultrasound examination, and histopathology. Inhibin concentration was measured by radioimmunoassay in serum before and after ACTH stimulation, and before and after treatment.

Results

In neutered dogs, median inhibin concentration was significantly higher in dogs with adrenocortical tumors (0.82 ng/mL) and PDH (0.16 ng/mL) than in dogs with PHEO and healthy dogs (both undetectable). Median inhibin concentration was significantly higher in dogs with adrenocortical tumors than in those with PDH and decreased after adrenalectomy. Median inhibin concentration was significantly higher in intact than in neutered healthy dogs and was similar in pre‐ and post‐ACTH stimulation. Sensitivity, specificity, and accuracy of serum inhibin concentration for identifying an adrenal tumor as a PHEO were 100, 88.9, and 93.6%, respectively.

Conclusions and Clinical Importance

Adrenocortical tumors and PDH but not PHEOs are associated with increased serum inhibin concentration; undetectable inhibin is highly supportive of PHEO in neutered dogs with adrenal tumors.     

Ultrasonographic adrenal gland measurements in clinically normal small breed dogs and comparison with pituitary-dependent hyperadrenocorticism

Ultrasonography is a sensitive and specific screening method for assessing the adrenal glands. The upper limit of the normal adrenal gland width is used as 7.5 mm. It is not known if adrenal gland width remains consistent with body weight. A reliable criterion of adrenal gland width in small breed dogs should be established. Small breed dogs with body weights of less than 10 kg were divided into two groups: 189 normal dogs and 22 dogs with pituitary-dependent hyperadrenocorticism (PDH). A retrospective study was conducted on dogs seen between January 1, 2006, and February 10, 2008. One hundred eighty-nine dogs of 14 different small breeds were enrolled in the normal adrenal gland group; the median gland width was 4.20 mm. Twenty-two dogs were in the PDH group; the median gland width was 6.30 mm. The cut-off value between normal adrenal glands and PDH was 6.0 mm. This figure gave a sensitivity and specificity of 75 and 94%, respectively, for detecting PDH. The adrenal gland appeared as a peanut shape with homogeneous hypoechoic parenchyma in normal dogs and in most dogs with PDH as well. This study was performed in a large population of small breed dogs and suggests that the normal adrenal gland size in small breed dogs is smaller than previously reported. We believe that a cut-off of 6.0 mm may be used as the criterion for differentiating a normal adrenal gland from adrenal hyperplasia.     

ULTRASONOGRAPHY OF ADRENAL GLANDS IN NORMAL FERRETS

The adrenal glands of 20 normal ferrets were imaged with ultrasound. Of the forty glands, only 4 (three right and one left) could not be clearly identified. Mean (±standard deviation) dimensions of the right (7.6 ± 1.8 mm length by 2.6 ± 0.4 mm width) and left (7.2 ± 1.8 mm length by 2.8 ± 0.5 mm width) glands were similar. Both adrenal glands were wider (p<0.05) sonographically in males than females. Measured length and width of the right gland positively correlated (p<0.05) with body weight. The glands had a hypoechoic outer zone and hyperechoic central region, were elongate to avoid in shape and located medial and, variably, at the level of the cranial pole of the ipsilateral kidney. This study demonstrates that normal adrenal glands can be imaged in ferrets.     

Ultrasonographic evaluation of the adrenal glands in six dogs with hypoadrenocorticism.

The purpose of this study was to determine the value of ultrasonographic characterization of the adrenal glands in dogs with hypoadrenocorticism. Measurements of adrenal glands were obtained in six dogs with hypoadrenocorticism. The adrenal glands on both sides were shorter (range: left adrenal gland length, 10.0 to 19.7 mm; right adrenal gland length, 9.5 to 18.8 mm) and thinner (range: left adrenal gland thickness, 2.2 to 3.0 mm; right adrenal gland thickness, 2.2 to 3.4 mm) than in normal dogs (range: left adrenal gland length, 13.2 to 26.3 mm; right adrenal gland length, 12.4 to 22.6 mm; left adrenal gland thickness, 3.0 to 5.2 mm; right adrenal gland thickness, 3.1 to 6.0 mm). Statistical analysis revealed a significant reduction in size of the left adrenal gland (p less than 0.05) in dogs with hypoadrenocorticism compared to the left adrenal gland in normal dogs. The results of this study show that atrophy of the adrenal glands in dogs with hypoadrenocorticism seems to lead to an ultrasonographic-measurable reduction in size of the adrenal glands.     

RETROSPECTIVE REVIEW OF THE ULTRASONOGRAPHIC FEATURES OF ADRENAL LESIONS IN 21 FERRETS

Clinical signs and follow-up information were recorded. Histopathologic diagnoses were obtained for 25 adrenal glands in 21 ferrets. Adrenal lesions included ten adenocarcinomas, nine adenomas, one hyperplasia and one cortical cyst. Four adrenal glands (all right-sided) were diagnosed as unspecified adrenal tumors but lacked a definite histopathologic diagnosis (adenoma vs. adenocarcinoma) due to incomplete surgical resection and consequent small sample sizes. Bilateral adrenal lesions were identified in 4 ferrets (19%). Adrenal shape, size, echogenicity, laterality, and the presence of vascular invasion were evaluated with ultrasound. Size and shape were variable and not specific to lesion type. Both benign and malignant adrenal tumors (adenomas, adenocarcinomas) appeared most often as masses with increased thickness and a normal length (11/23), less frequently as larger masses with increased thickness and length (4/23) or as nodules focally deforming the normal adrenal shape (6/23). The only cortical cyst appeared as a nodule. Three adrenal glands had a normal size and shape and were diagnosed as adenomas (2) or hyperplasia (1). Therefore treatment may be warranted based solely on clinical signs if adrenal glands are ultrasonographically normal. Vascular invasion was not identified ultrasonographically. However, focal absence of periglandular fat resulting in contact of 8 adrenal glands with either caudal vena cava (6), aorta (1) or liver (1) identified ultrasonographically, correlated with incomplete surgical resectability (6/8) and histopathologic diagnoses of carcinoma (4/8) or unspecified tumors (4/8). Therefore, a focal absence of periglandular fat between the adrenal gland and the large vessels or liver, deviation or compression of the large vessels by the adrenal lesion may indicate malignancy. Adrenal tumors (benign and malignant) were often associated with a prominent uterus, uterine stump or prostate with or without prostatic cysts.     

ULTRASONOGRAPHIC EVALUATION OF ADRENAL GLAND SIZE COMPARED TO BODY WEIGHT IN NORMAL DOGS

The accepted cut‐off value for adrenal gland maximum diameter of 0.74 cm to distinguish adrenal gland enlargement in dogs regardless of body weight may not be appropriate for small to medium breed dogs. The purpose of the current retrospective study was to examine adrenal gland dimensions as a function of body weight in healthy dogs in three weight categories (< 10 kg, 10–30 kg, and > 30 kg) representing small, medium, and large breeds, respectively, to establish greater confidence in determining if adrenal gland size is abnormal. The measurements of length (sagittal plane), cranial and caudal pole thickness (sagittal and transverse planes), and caudal pole width (transverse plane) of both adrenal glands were obtained ultrasonographically in clinically healthy dogs (n = 45) with 15 dogs in each weight group. Findings support our hypothesis that adrenal gland size correlates with body weight in normal dogs, and more precise reference intervals should be created for adrenal gland size by categorizing dogs as small, medium, or large breed. The caudal pole thickness of either adrenal gland in a sagittal plane was the best dimension for evaluating adrenal gland size based on low variability, ease, and reliability in measurement.     

Nephrotomography and ultrasonography for the localization of hyperfunctioning adrenocortical tumors in dogs

Nephrotomography and ultrasonography were used in 11 dogs with hyperadrenocroticism to assess the value of these techniques for the localization of biochemically diagnosed hyperfunctioning adrenocortical tumors. Both techniques enabled accurate localization of a unilateral adrenal mass in each of the dogs. Cross-sectional diameters of the masses ranged from 1 to 4 cm. In 1 dog, expansion of tumor into the caudal vena cava was revealed by caudal venacavography and ultrasonography. Mineralization in the tumor mass in 2 dogs was easily recognized by nephrotomography, but not by ultrasonography. Paracostal laparotomy confirmed the presence of an adrenocortical tumor in each dog, and expansion of tumor into the caudal vena cava in 1 dog. Cross-sectional diameters of the tumors ranged from 1.2 to 4.5 cm and corresponded well with cross-sectional measurements by nephrotomography and ultrasonography. It was concluded that nephrotomography and ultrasonography have similar diagnostic accuracies for the detection and localization of hyperfunctioning adrenocortical tumors.     

Elective and emergency surgical management of adrenal gland tumors: 60 cases (1999-2006)

Sixty-one adrenal gland tumors were surgically removed from 60 dogs. Fifty-two dogs underwent elective adrenalectomy and 8 dogs underwent emergency adrenalectomy for acute adrenal hemorrhage. Size of adrenal tumors ranged from 10 mm to 80 mm. Histopathology confirmed a diagnosis of adrenocortical tumor in 47 dogs, 26 of which were malignant. Pheochromocytoma was diagnosed in 11 dogs. Six dogs had tumor invasion of the caudal vena cava. Of the seven dogs that did not survive the perioperative period, four underwent emergency adrenalectomy. No dogs with tumor invasion of the caudal vena cava died perioperatively. Perioperative morality rates were 5.7% for dogs that underwent elective adrenalectomy and 50% for dogs that underwent emergency adrenalectomy for acute adrenal hemorrhage. Median survival time was 492 days for the 53 dogs that survived the perioperative period. Of the factors analyzed, only adrenal tumor size and the presence of acute adrenal hemorrhage had predictive values for perioperative mortality. Those dogs that survived the perioperative period had extended survival times of up to 1,590 days. The mortality rate associated with elective adrenalectomy in dogs may be lower than previously reported. Dogs with very large tumors or acute adrenal hemorrhage may have a more guarded prognosis.     

Surgical treatment and long-term outcome of ferrets with bilateral adrenal tumors or adrenal hyperplasia: 56 cases (1994-1997).

OBJECTIVE: To determine signalment, clinical signs, concurrent diseases, response to surgical treatment, and long-term outcome of ferrets with bilateral adrenal tumors or adrenal hyperplasia. DESIGN: Retrospective study. ANIMALS: 56 ferrets with bilateral adrenal tumors or adrenal hyperplasia confirmed histologically following subtotal bilateral adrenalectomy. PROCEDURE: Medical records of all ferrets with bilateral adrenal tumors or hyperplasia examined between 1994 and 1997 were reviewed. Ferrets underwent a subtotal bilateral adrenalectomy or a unilateral adrenalectomy initially, followed by a unilateral subtotal adrenalectomy when tumors or hyperplasia later developed on the contralateral adrenal gland. A long-term follow-up of a minimum of 18 months after final adrenal gland surgery was obtained by examination of medical records and follow-up telephone conversations. RESULTS: Clinical signs of hyperadrenocorticism included bilaterally symmetric alopecia, return to male sexual behavior in castrated male ferrets, or swollen vulva in spayed female ferrets. Surgical treatment of bilateral adrenal disease by subtotal bilateral adrenalectomy (or unilateral adrenalectomy followed by contralateral unilateral subtotal adrenalectomy) was effective with a mortality rate of < 2%. Only 3 (5%) ferrets required glucocorticoid or mineralocorticoid replacement following subtotal bilateral adrenalectomy. Recurrence after bilateral adrenalectomy was 15% with a mean long-term follow-up period of 30 months. CONCLUSIONS AND CLINICAL RELEVANCE: Bilaterally symmetric alopecia, return to male sexual behavior in castrated male ferrets, or swollen vulva in spayed female ferrets are indicative of adrenal tumors or adrenal hyperplasia in ferrets. Surgical treatment of bilateral adrenal disease by subtotal bilateral adrenalectomy is effective, with a low rate of complications and postoperative recurrence rate.     

ADRENAL ULTRASONOGRAPHY IN THE DOG

The ultrasonographic appearance of the normal canine adrenal gland has not been described. This is due to the small size and shape of the canine adrenal glands, overlying abdominal viscera, similar acoustic texture to that of the surrounding tissue, frequent abundant perirenal fat, and the lack of patient compliance. Adrenal enlargement in association with hyperadrenocorticism, secondary to hyperplasia or neoplasia, can sometimes be identified by finding a distinct structure cranial and/or medial to the cranial pole of either kidney. Case history reports are used to characterize the appearance of adrenal enlargement from hyperplasia and adrenocortical adenocarcinoma. Additional case history reports are included to illustrate possible interpretation problems. Lack of ultrasonographic visualization of the adrenal gland does not rule out the possibility of enlargement, particularly if the enlargement in mild.     

Evaluation of a comparative pathogenesis between cancer-associated retinopathy in humans and sudden acquired retinal degeneration syndrome in dogs via diagnostic imaging and western blot analysis

OBJECTIVE: To evaluate dogs with sudden acquired retinal degeneration syndrome (SARDS) for evidence of pituitary gland, adrenal gland, and pulmonary neoplasia and antiretinal antibodies and to evaluate dogs with neoplasia for antiretinal antibodies. ANIMALS: 57 clinically normal dogs, 17 with SARDS, and 53 with neoplasia. PROCEDURE: Thoracic radiography, ultrasonography of adrenal glands, and contrast-enhanced computed tomography of pituitary glands were performed in 15 dogs with SARDS. Western blot analysis was performed on sera of all dogs; recoverin (23 kd) and arrestin (48 kd) retinal antibodies were used as positive controls. RESULTS: Neoplasia was not detected via diagnostic imaging in dogs with SARDS. Western blot analysis revealed bands in all dogs ranging from > 48 to < 23 kd. Prominent bands with equivalent or greater density than 1 or both positive controls at the 1:1,000 dilution, and present at the 1:3,000 dilution, were detected in 28% of clinically normal dogs, 40% of dogs with neoplasia, and 41% of dogs with SARDS. No bands in dogs with SARDS had a consistent location of immune activity, and none were detected at the 23-kd site. The area around the 48-kd site had increased immune activity in all 3 groups. CONCLUSIONS AND CLINICAL RELEVANCE: The etiology of SARDS in dogs does not appear to be similar to cancer-associated retinopathy in humans on the basis of absence of differential antibody activity against retinal proteins. Although dogs with SARDS often have clinical signs compatible with hyperadrenocorticism, neoplasia of the adrenal glands, pituitary gland, or lungs was not detected.     

Evaluating the correlation between adrenal gland dimensions and aortic diameter in healthy dogs

In the present study, the relationship of normal adrenal dimensions with weight, aortic diameter, age and sex was evaluated. Moreover, a formula for estimating the normal dimensions of adrenal gland was provided. Thirty‐two intact adult dogs that were considered healthy based on history, physical examination, routine blood works and specific adrenal tests as well as absence of any abnormal ultrasonographic findings were included. Adrenal glands and abdominal aorta were imaged in the sagittal plane by ultrasound. Length, maximal height of the cranial and caudal poles, area and circumference of the left and right adrenal glands and also the internal diameter of the abdominal aorta were measured. Analysis showed that there is a positive correlation between the adrenal gland dimensions and weight and aortic diameter. The ratio of adrenal gland dimensions and the aortic diameter was calculated, but this ratio showed a great amount of variability in tandem with a significant correlation to the weight; Meaning that the ratio of the adrenal gland dimensions to the aortic diameter was not a reliable index for evaluating the size of the normal adrenal gland in animals with different weights. Therefore, we used the weight along with adrenal measurements in a linear regression model, and then, we were able to estimate the adrenal gland dimensions in different weights. Knowing the relationship of normal adrenal dimensions with the indices such as weight, age, sex and diameter of abdominal aorta can help the clinicians to diagnose the adrenal gland diseases.     

Surgical management of adrenal gland tumors with and without associated tumor thrombi in dogs: 40 cases (1994-2001)

OBJECTIVE: To compare pathologic findings and results of adrenalectomy for adrenal gland tumors in dogs with and without vena caval tumor thrombi. DESIGN: Retrospective study. ANIMALS: 40 dogs with adrenal gland tumors. PROCEDURE: Medical records were examined. An exact logistic regression analysis was used to evaluate associations between tumor type or right-sided versus left-sided tumor involvement and development of caval tumor thrombi and associations between tumor thrombi, tumor type, or right- versus left-sided location and perioperative complications and mortality rate. Survival was compared between dogs with and without tumor thrombi. RESULTS: Caval thrombi were detected in 25% of dogs, including 3 of 28 (11%) dogs with an adrenocortical tumor and 6 of 11 dogs with a pheochromocytoma. A caval tumor thrombus was detected in 6 of 17 right-sided and 4 of 20 left-sided tumors. Sensitivity and specificity of abdominal ultrasonography for detection of caval thrombi were 80 and 90%, respectively. Intraoperative and postoperative complications developed in 15 and 51% of dogs, respectively. The mortality rate was 22%. There were no significant differences in perioperative morbidity and mortality rates between dogs with and without tumor thrombi. CONCLUSIONS AND CLINICAL RELEVANCE: Caval thrombi associated with adrenal gland tumors are amenable to adrenalectomy and thrombectomy without significantly increased perioperative morbidity and mortality rates, assuming the surgeon is experienced in appropriate techniques.     

Canine Hyperadrenocorticism Due to Adrenocortical Neoplasia: Pretreatment Evaluation of 41 Dogs

This retrospective study identifies parameters that might separate dogs with hyperadrenocorticism caused by adrenocortical tumors from dogs with pituitary-dependent hyperadrenocorticism. Further, an attempt was made to identify factors that could separate dogs with adrenocortical adenomas from dogs with carcinomas. The records of 41 dogs with hyperadrenocorticism caused by adrenocortical neoplasia were reviewed. The history, physical examination, urinalysis, hemogram (CBC), chemistry profile adrenocorticotrophic hormone (ACTH) stimulation and low dose dexamethasone test results were typical of the nonspecific diagnosis of hyperadrenocorticism. The preceding information on the 41 dogs with adrenocortical tumors was compared with that from 44 previously diagnosed pituitary-dependent hyperadrenocorticoid dogs. There was no parameter which aided in separating these two groups of dogs. Thirty dogs with adrenocortical tumors were tested with a high-dose dexamethasone test and none had suppressed plasma cortisol concentrations 8 hours after IV administration of 0.1 mg/kg of dexamethasone. In 29 of the 41 adrenal tumor dogs, plasma endogenous ACTH was not detectable on at least one measurement (less than 20 pg/ml). The remaining 12 dogs from this group had nondiagnostic concentrations (20-45 pg/ml). Thirteen of 22 dogs (59%) with adrenocortical carcinomas had adrenal masses identified on abdominal radiographs and seven of 13 dogs (54%) with adrenocortical adenomas had radiographically visible adrenal masses. Thirteen of 17 adrenocortical carcinomas (76%) and five of eight adenomas (62%) were identified with ultrasonography. Radiographs of the thorax and ultrasonography of the abdomen identified most of the dogs (8 of 11) with metastatic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Laparoscopic adrenalectomy for treatment of unilateral adrenocortical carcinomas: technique, complications, and results in seven dogs

Objective— To investigate the feasibility of, and outcome after, laparoscopic adrenalectomy in dogs with unilateral adrenocortical carcinoma.
Study Design— Case series.
Animals— Dogs (n=7) with Cushing's syndrome caused by unilateral adrenocortical carcinoma.
Methods— Laparoscopic adrenalectomy with the dog in lateral recumbency on the unaffected side. Three 5-mm portals (1 laparoscopic portal, 2 instrument portals) were placed in the paralumbar fossa. A fourth instrumental portal (5–12 mm) was placed above the kidney. After dissection and hemostatic control of the phrenicoabdominal vein, the adrenal gland was carefully dissected or when there was capsule fragility, necrotic content was partially aspirated. The remaining glandular tissue was removed through the 12-mm trocar site.
Results— Dogs with unilateral adrenocortical carcinoma (3 right-sided, 4 left-sided) without invasion of the caudal vena cava were successfully operated by laparoscopic approach. There were no significant intraoperative complications; 2 dogs died within 48 hours of surgery because of respiratory complications. Five dogs were discharged 72 hours after surgery, and signs of hyperadrenocorticism disappeared thereafter (survival time ranged from 7 to 25 months).
Conclusions— Laparoscopic adrenalectomy is feasible in dogs with either right- or left-sided adrenocortical carcinoma not involving the caudal vena cava.
Clinical Relevance— When performed by experienced surgeons, laparoscopic adrenalectomy offers a minimally invasive alternative to open laparotomy or retroperitoneal surgery for the treatment of unilateral adrenocortical carcinoma in dogs.     

Accuracy of Ultrasonographic Measurements of Adrenal Glands in Dogs: Comparison with Necroscopic Findings

Ultrasonographic evaluation of the adrenal glands was performed in 85 dogs, followed by macroscopic and histopathological examination either post‐mortem or after adrenalectomy. This retrospective cross‐sectional study evaluated the difference between gross and ultrasonographic measurements to determine the diagnostic accuracy of ultrasonography in the evaluation of canine adrenal gland size. The differences were assessed for gland length, thickness at cranial, middle and caudal regions, and surface area. In our sample, ultrasound error accuracy ranged between 0% in measurement of the right adrenal gland surface area and 25.21% for left cranial pole thickness. The parameters with minor errors were caudal pole thickness (3.64% right side and 3.49% left side) and length (5.75% right side and 2.19% left side). The ultrasonographic measurements generally underestimated the actual size of the adrenal glands. No statistically significant differences were observed for measurement errors between normal and pathological adrenal glands. This study confirmed that the caudal pole of both glands is the best parameter for ultrasonographic evaluation of normal and pathological adrenal glands size in dog. Furthermore, the surface area could be considered as a dimensional parameter for better assessment of the complex shape and the global aspect of the adrenal glands, while standardize ultrasonographic projections are needed to measure the cranial pole of both adrenal glands.     

CONTRAST-ENHANCED ULTRASONOGRAPHY FOR CHARACTERIZATION OF CANINE FOCAL LIVER LESIONS

In six normal beagles and 27 dogs with spontaneous focal or multifocal liver lesions, contrast-enhanced ultrasonography using Sonazoid^® was performed. Sonazoid^® is a newly developed second-generation contrast agent with the ability to be used for real-time contrast imaging along with parenchymal imaging. An appropriate protocol for the evaluation of all three phases (arterial, portal, and parenchymal) was established based on the results for normal beagles. By evaluation of the echogenicity of hepatic nodules during the arterial and parenchymal phases it was possible to differentiate malignant tumors from benign nodules with very high accuracy. In 15 of 16 dogs diagnosed as malignant tumors, nodules were clearly hypoechoic to the surrounding normal liver during the parenchymal phase. Additionally, malignant tumors had different echogenicity compared with the surrounding normal liver during the arterial phase in 14 of 15 dogs. In the portal phase, there were no characteristic findings. Contrast-enhanced ultrasonography with Sonazoid^® appears to improve the characterization of canine focal and multifocal hepatic lesions.     

Effect of mitotane on pituitary corticotrophs in clinically normal dogs

OBJECTIVE: To evaluate the effects of mitotane administration on the function and morphology of pituitary corticotrophs in clinically normal dogs. ANIMALS: 12 clinically normal adult Beagles. PROCEDURES: Dogs were randomly assigned to the control group or the mitotane treatment group. In mitotane treatment group dogs, mitotane was administered for 1 month. In both groups, ACTH stimulation testing and corticotrophin-releasing hormone (CRH) stimulation testing were performed. Magnetic resonance imaging (MRI) of the pituitary gland and brain was performed in mitotane treatment group dogs before and after administration of mitotane. After CRH stimulation testing and MRI, dogs were euthanatized and the pituitary gland and adrenal glands were excised for gross and histologic examination. RESULTS: ACTH concentrations in mitotane treatment group dogs were significantly higher than in the control group dogs following CRH stimulation. Magnetic resonance imaging revealed that pituitary glands were significantly larger in treatment group dogs after administration of mitotane, compared with before administration. On gross and histologic examinations, the adrenal cortex was markedly atrophied. Immunohistochemistry revealed hypertrophy of corticotrophs in pituitary glands of mitotane treatment group dogs. CONCLUSIONS AND CLINICAL RELEVANCE: These findings indicate that inhibition of the adrenal cortex by continuous administration of mitotane leads to functional amplification and morphologic enhancement of corticotrophs in clinically normal dogs. In instances of corticotroph adenoma, hypertrophy of individual corticotrophs induced by mitotane may greatly facilitate enlargement of the pituitary gland and increases in ACTH secretion.